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目的 探讨百日咳菌液诱导的急性感染性脑水肿的发生机制和类型 ,并观察尼莫地平和MK - 80 1的作用。方法 测定脑组织水分含量和EB含量 ,Fura 2 /AM测定突触体 [Ca2 + ]i,放射性配基结合法测定NMDA受体的结合量。结果 [Ca2 + ]i随脑水肿时间的延长而持续进行性升高 ,伴随脑组织水分含量和EB含量增加。MK 80 1预处理和尼莫地平治疗后 ,脑组织含水量和EB含量及[Ca2 + ]i明显下降 (P <0 0 5 )。PB组与NS组相比Kd值有显著性差异 ,而Bmax差异无显著性。结论 感染性脑水肿是混合性脑水肿 ,它的发生与Ca2 + 通道开放和NMDA受体介导的迟发性钙离子内流及BBB通透性增加密切相关。MK 80 1和尼莫地平通过缓解细胞内钙离子超载和改善BBB的通透性 ,从而减轻脑水肿。
Objective To investigate the mechanism and type of acute infectious cerebral edema induced by pertussis bacilli and to observe the effect of nimodipine and MK - 80 1. Methods The brain water content and EB content were measured. Fura 2 / AM was used to measure the synaptosomal [Ca 2+] i. The binding of NMDA receptor was measured by radioligand binding assay. Results [Ca2 +] i continued to progressively increase with the time of cerebral edema, with the increase of brain water content and EB content. MK 80 1 pretreatment and nimodipine treatment, brain water content and EB content and [Ca2] i significantly decreased (P <0 05). There was a significant difference in Kd between PB group and NS group, but Bmax had no significant difference. Conclusions Infectious brain edema is a mixed brain edema. Its occurrence is closely related to the opening of Ca2 + channels and NMDA receptor - mediated delayed calcium influx and BBB permeability increase. MK 80 1 and nimodipine reduce cerebral edema by alleviating intracellular calcium overload and improving BBB permeability.